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Molecular Pharmacology

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Abstract

Mechanisms of sensitivity and natural resistance to antifolates in a methylcholanthrene-induced rat sarcoma.

W W Li, J T Lin, B I Schweitzer and J R Bertino
Molecular Pharmacology November 1991, 40 (5) 854-858;
W W Li
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J T Lin
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B I Schweitzer
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J R Bertino
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Abstract

A methylcholanthrene-induced rat sarcoma that can be propagated in vitro or in vivo was evaluated for resistance to antifolates and was found to be relatively resistant to methotrexate and 10-ethyl-10-deazaaminopterin but sensitive to trimetrexate. Rat sarcoma cell extracts contained low levels of dihydrofolate reductase activity, the target enzyme of methotrexate, and inhibition of this enzyme by these three antifolates was similar. Transport studies showed poor uptake of both methotrexate and 10-ethyl-10-deazaaminopterin. In contrast, trimetrexate achieved high intracellular levels. The poor uptake of methotrexate was not due to lack of polyglutamylation. Thus, the basis for natural resistance to methotrexate and 10-ethyl-10-deazaaminopterin, compared with trimetrexate, in this rat sarcoma cell line was due to decreased transport of these drugs.

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Molecular Pharmacology
Vol. 40, Issue 5
1 Nov 1991
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Abstract

Mechanisms of sensitivity and natural resistance to antifolates in a methylcholanthrene-induced rat sarcoma.

W W Li, J T Lin, B I Schweitzer and J R Bertino
Molecular Pharmacology November 1, 1991, 40 (5) 854-858;

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Abstract

Mechanisms of sensitivity and natural resistance to antifolates in a methylcholanthrene-induced rat sarcoma.

W W Li, J T Lin, B I Schweitzer and J R Bertino
Molecular Pharmacology November 1, 1991, 40 (5) 854-858;
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